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Objective: The prevalence of Adult attention deficit-hyperactivity disorder (A-ADHD) has been estimated to be 5%. There are several hypotheses regarding the etiology of ADHD. Although numerous researches have been conducted regarding neurobiology of pediatric ADHD, A-ADHD studies were relatively few. Many studies have indicated that oxidant mediated neuronal damage might play a role in the pathophysiology of various psychiatric disorders. Recently, oxidative stress has been studied in A-ADHD and there is an accumulating evidence to support its’ role. We have previously reported that oxidants were high and antioxidant levels were low in A-ADHD. In the present study, we evaluated jointly whether catalase (CAT), an antioxidant, activity and thiol, an oxidant, levels are associated with A-ADHD or not. We expect to find the clues of oxidative imbalance more remarkably, since the nature of disease interferes more with brain related functions.
Methods: Twenty-five A-ADHD patients from Gaziantep University, diagnosed according to Turgay’s Turkish version of Adult ADD/ADHD DSM IV-Based Diagnostic Screening and Rating Scale by two psychiatrists, and 25 healthy volunteer controls were included. The subjects strictly refrained from any substance intake and physical exercise after 08:00 p.m. on the day before collection. CAT and thiol were measured in plasma samples of study groups.
Results: Age, gender, and BMI index of patients and controls have shown homogeneity and there were no differences between the groups. Total score and subscores were not correlated with any of the mentioned biochemical parameters. The mean CAT levels in patients with ADHD were significantly higher and thiol levels were lower than those of controls (<0.001, <0.001, respectively). The patients, who had a comorbid psychiatric disorder exhibited significantly higher CAT and significantly lower thiol levels compared with patients, who had only ADHD.
Conclusions: In a previous study of ours, we found that A-ADHD patients’ Total Antioxidant Status (TAS) were higher than controls and we interpreted this finding as a “rebound phenomenon” to the increased oxidative stress. Thus, we may also make the same interpretation to the present study findings. On the other hand, we found that A-ADHD patients had lower oxidants (thiol) level than controls. In a recent study that included the pediatric ADHD patients thiol levels were found higher in the ADHD group than the controls but the difference was not statistically significant. Malondialdehyde (MDA) and nitric oxide (NO), indicators of oxidative stress, were significantly lower in the pediatric ADHD group than the control group. Taken together with CAT results thiol levels might be decreased by increasing the antioxidant level. There is an equilibrium between oxidants and antioxidants thus, if antioxidant level increases, oxidants should be decreased secondarily. What we have seen from our results was this equilibrium. The etiology of ADHD is related with the alteration on dopaminergic activation and hypofunction of dopamine pathways. Dopamine is very susceptible to auto-oxidation when antioxidant defense is weak. Therefore, oxidative stress may be involved in dopaminergic pathways in A-ADHD. However, the exact relationship between oxidative stress and A-ADHD remains unclear and there is a need for further studies on this field.